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Title: The effects of diclofenac and ibuprofen on heart function and oxidative stress markers in the isolated rat heart
Authors: Jevdjević M.
Srejovic I.
Zivkovic V.
Barudzic N.
Petkovic, Anica
Bradic, Jovana
Djuric D.
Jakovljevic V.
Issue Date: 2014
Abstract: Eicosanoids lead to the promotion of inflammation, cause fever and pain and have many other effects. NSAIDs block the action of cyclooxygenase (COX) during the process of converting arachidonic acid into inflammatory mediators, thus reducing the symptoms of inflammation. Investigations focusing on nonselective COX inhibitors, used in high doses, revealed harmful effects on myocardial function. The aim of our study was to assess the effects of two nonselective NSAIDs, diclofenac and ibuprofen, on cardiodynamic parameters, coronary flow and oxidative stress biomarkers in isolated rat hearts. The hearts of male Wistar albino rats were excised and retrogradely perfused according to the Langendorff technique at gradually increased coronary perfusion pressures (40-120 cm H2O). The experiments were performed under controlled conditions (Krebs-Henseleit physiological solution). The hearts were perfused with 10μmol/l diclofenac and 10 μmol/l ibuprofen. The heart function parameters, including the maximum rate of pressure development (dp/dt max), minimum rate of pressure development (dp/dt min), systolic left ventricular pressure (SLVP), diastolic left ventricular pressure (DLVP), mean perfusion pressure (MBP) and heart rate (HR), were continuously registered. Coronary flow (CF) was measured flow metrically. Oxidative stress markers, including the index of lipid peroxidation measured as TEARS, nitric oxide measured through nitrites (N02), super oxide anion radical (02), and hydrogen peroxide (H202 in the coronary venous effluent, were assessed spectrophotometrically. Our results showed that diclofenac affected cardiodynamic parameters more signifi cantly than did ibuprofen. Furthermore, the present data indicate that both estimated COX inhibitors do not promote the production of reactive oxygen species.
Type: article
DOI: 10.2478/SJECR-2014-0002
ISSN: 1820-8665
SCOPUS: 2-s2.0-84898718580
Appears in Collections:Faculty of Medical Sciences, Kragujevac

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